high (>0.60) and the total genetic variance of each criteria attributable to the factor ranged from 38% for ‘craving’ to 89% for ‘failure to fulfill major roles’ (see Table 4 for a summary of factor loadings and percent variance explained in the EGFA). Our analysis of competing models of additive genetic effects on AUD indicated that the model containing a single genetic factor provided the best fit to the data (χ2=49905.53, degrees of freedom (df)=44, AIC=49817.53). On the contrary, the two-factor genetic model that allowed for a correlation between the genetic factors was less parsimonious (compared to the one-factor model: ΔAIC=4046.55), but estimated the correlation between the abuse and dependence factors at 1.00 [95% confidence interval=0.99, 1.00]. We also examined a bi-genetic factor model that allowed craving to cross-load across the factors; results were similar and this adjusted model fit the data slightly worse (compared to the one-factor model: ΔAIC=4048.55). Overall, both the EGFA and CFA suggest shared additive genetic effects across symptoms of DSM-5 AUD.
